Chlamydia trachomatis is the most common bacterial sexually transmitted infection in the developed world with 2-3 million actively-infected individuals in the U.S. (Prevention, 2007) and similar numbers in Europe (Low, 2004). In women C. trachomatis infections can ascend into the upper reproductive tract causing pelvic inflammatory disease and scarring with resulting infertility and ectopic pregnancies. Standard public health measures including provision of antibiotic therapy and partner tracing have not significantly decreased the incidence of C. trachomatis infections. There is a general consensus among Chlamydia basic scientists and clinicians that development of a Chlamydia vaccine is a health care priority.
Unfortunately our understanding of the immunobiology of T cell interactions with Chlamydia-infected epithelial cells is limited, and most of the existing studies are limited by the use of epithelial tumors as antigen presenting cells (APC). While tumor cell lines have morphologic features consistent with an epithelial lineage, it is unclear whether their immunobiology remains intact after tumorgenesis and evasion of host immunosurveillance. Understanding cellular immunity at the epithelial interface is critical for developing new vaccine strategies and identifying surrogate markers for vaccine efficacy prior to initiating clinical trials.
Given the huge impact that infections with Chlamydia has on human health and the problems with currently available treatments for and vaccinations against this pathogen, there is a pressing need for increased understanding of how the mammalian immune system interacts with this pathogen. Some aspects and embodiments of the invention address these needs.